Dr. Padma Garvey, a gynecologist working in New York’s Hudson Valley (about 75 miles outside of New York City), has come to be known as “the plant-based doctor mom” for her outspoken advocacy of a whole-food, plant-based diet both in... Read more

Why is meat consumption a risk factor for diabetes? Why does there appear to be a stepwise reduction in diabetes rates as meat consumption drops? Instead of avoiding something in meat, it may be that people are getting something protective from plants. Free radicals may be an important trigger for insulin resistance, and antioxidants in plant foods may help. Put people on a plant-based diet, and their antioxidant enzymes shoot up. So not only do plants provide antioxidants, but may boost our own anti-endogenous antioxidant defenses, whereas, on the conventional diabetic diet, they get worse.

In my video, How May Plants Protect Against Diabetes, I discuss how there are phytonutrients in plant foods that may help lower chronic disease prevalence by acting as antioxidants and anti-cancer agents, and by lowering cholesterol and blood sugar. Some, we're now theorizing, may even be lipotropes, which have the capacity to hasten the removal of fat from our liver and other organs, counteracting the inflammatory cascade believed to be directly initiated by saturated-fat-containing foods. Fat in the bloodstream--from the fat on our bodies or the fat we eat--not only causes insulin resistance, but also produces a low-grade inflammation that can contribute to heart disease and non-alcoholic fatty liver disease.

Fiber may also decrease insulin resistance. One of the ways it may do so is by helping to rid the body of excess estrogen. There is strong evidence for a direct role of estrogens in the cause of diabetes, and it's been demonstrated that certain gut bacteria can produce estrogens in our colon. High-fat, low-fiber diets appear to stimulate the metabolic activity of these estrogen-producing intestinal bacteria. This is a problem for men, too. Obesity is associated with low testosterone levels and marked elevations of estrogens produced not only by fat cells but also by some of the bacteria in our gut. Our intestinal bacteria may produce these so-called diabetogens (diabetes-causing compounds) from the fats we eat. By eating lots of fiber, though, we can flush this excess estrogen out of our bodies.

Vegetarian women, for example, excrete two to three times more estrogens in their stools than omnivorous women, which may be why omnivorous women have 50% higher estrogen blood levels. These differences in estrogen metabolism may help explain the lower incidence of diabetes in those eating more plant-based diets, as well as the lower incidence of breast cancer in vegetarian women, who get rid of twice as much estrogen because they get rid of twice as much daily waste in general.

Either way, "[m]eat consumption is consistently associated with diabetes risk. Dietary habits are readily modifiable, but individuals and clinicians will consider dietary changes only if they are aware of the potential benefits of doing so." The identification of meat consumption as a risk factor for diabetes provides helpful guidance that sets the stage for beneficial behavioral changes. Meat consumption is something doctors can easily ask about, and, once identified, at-risk individuals can then be encouraged to familiarize themselves with meatless options.

Why is meat consumption a risk factor for diabetes? Why does there appear to be a stepwise reduction in diabetes rates as meat consumption drops? Instead of avoiding something in meat, it may be that people are getting something protective from plants. Free radicals may be an important trigger for insulin resistance, and antioxidants in plant foods may help. Put people on a plant-based diet, and their antioxidant enzymes shoot up. So not only do plants provide antioxidants, but may boost our own anti-endogenous antioxidant defenses, whereas, on the conventional diabetic diet, they get worse.

In my video, How May Plants Protect Against Diabetes, I discuss how there are phytonutrients in plant foods that may help lower chronic disease prevalence by acting as antioxidants and anti-cancer agents, and by lowering cholesterol and blood sugar. Some, we're now theorizing, may even be lipotropes, which have the capacity to hasten the removal of fat from our liver and other organs, counteracting the inflammatory cascade believed to be directly initiated by saturated-fat-containing foods. Fat in the bloodstream--from the fat on our bodies or the fat we eat--not only causes insulin resistance, but also produces a low-grade inflammation that can contribute to heart disease and non-alcoholic fatty liver disease.

Fiber may also decrease insulin resistance. One of the ways it may do so is by helping to rid the body of excess estrogen. There is strong evidence for a direct role of estrogens in the cause of diabetes, and it's been demonstrated that certain gut bacteria can produce estrogens in our colon. High-fat, low-fiber diets appear to stimulate the metabolic activity of these estrogen-producing intestinal bacteria. This is a problem for men, too. Obesity is associated with low testosterone levels and marked elevations of estrogens produced not only by fat cells but also by some of the bacteria in our gut. Our intestinal bacteria may produce these so-called diabetogens (diabetes-causing compounds) from the fats we eat. By eating lots of fiber, though, we can flush this excess estrogen out of our bodies.

Vegetarian women, for example, excrete two to three times more estrogens in their stools than omnivorous women, which may be why omnivorous women have 50% higher estrogen blood levels. These differences in estrogen metabolism may help explain the lower incidence of diabetes in those eating more plant-based diets, as well as the lower incidence of breast cancer in vegetarian women, who get rid of twice as much estrogen because they get rid of twice as much daily waste in general.

Either way, "[m]eat consumption is consistently associated with diabetes risk. Dietary habits are readily modifiable, but individuals and clinicians will consider dietary changes only if they are aware of the potential benefits of doing so." The identification of meat consumption as a risk factor for diabetes provides helpful guidance that sets the stage for beneficial behavioral changes. Meat consumption is something doctors can easily ask about, and, once identified, at-risk individuals can then be encouraged to familiarize themselves with meatless options.

We've known that being overweight and obese are important risk factors for type 2 diabetes, but, until recently, not much attention has been paid to the role of specific foods. I discuss this issue in my video, Why Is Meat a Risk Factor for Diabetes?

A 2013 meta-analysis of all the cohorts looking at the connection between meat and diabetes found a significantly higher risk associated with total meat consumption--especially consumption of processed meat, particularly poultry. But why? There's a whole list of potential culprits in meat: saturated fat, animal fat, trans fats naturally found in meat, cholesterol, or animal protein. It could be the heme iron found in meat, which can lead to free radicals and iron-induced oxidative stress that may lead to chronic inflammation and type 2 diabetes, or advanced glycation end (AGE) products, which promote oxidative stress and inflammation. Food analyses show that the highest levels of these so-called glycotoxins are found in meat--particularly roasted, fried, or broiled meat, though any foods from animal sources (and even high fat and protein plant foods such as nuts) exposed to high dry temperatures can be potent sources of these pro-oxidant chemicals.

In another study, researchers fed diabetics glycotoxin-packed foods, like chicken, fish, and eggs, and their inflammatory markers--tumor necrosis factor, C-reactive protein, and vascular adhesion molecules--shot up. "Thus, in diabetes, environmental (dietary) AGEs promote inflammatory mediators, leading to tissue injury." The good news is that restriction of these kinds of foods may suppress these inflammatory effects. Appropriate measures to limit AGE intake, such as eliminating meat or using only steaming and boiling as methods for cooking it, "may greatly reduce the already heavy burden of these toxins in the diabetic patient." These glycotoxins may be the missing link between the increased consumption of animal fat and meats and the development of type 2 diabetes.

Since the 2013 meta-analysis was published, another study came out in which approximately 17,000 people were followed for about a dozen years. Researchers found an 8% increased risk for every 50 grams of daily meat consumption. Just one quarter of a chicken breast's worth of meat for the entire day may significantly increase the risk of diabetes. Yes, we know there are many possible culprits: the glycotoxins or trans fat in meat, saturated fat, or the heme iron (which could actually promote the formation of carcinogens called nitrosamines, though they could also just be produced in the cooking process itself). However, we did learn something new: There also appears to be a greater incidence of diabetes among those who handle meat for a living. Maybe there are some diabetes-causing zoonotic infectious agents--such as viruses--present in fresh cuts of meat, including poultry.

A "crucial factor underlying the diabetes epidemic" may be the overstimulation of the aging enzyme TOR pathway by excess food consumption--but not by the consumption of just any food: Animal proteins not only stimulate the cancer-promoting hormone insulin growth factor-1 but also provide high amounts of leucine, which stimulates TOR activation and appears to contribute to the burning out of the insulin-producing beta cells in the pancreas, contributing to type 2 diabetes. So, it's not just the high fat and added sugars that are implicated; critical attention must be paid to the daily intake of animal proteins as well.

According to a study, "[i]n general, lower leucine levels are only reached by restriction of animal proteins." To reach the leucine intake provided by dairy or meat, we'd have to eat 9 pounds of cabbage or 100 apples to take an extreme example. That just exemplifies the extreme differences in leucine amounts provided by a more standard diet in comparison with a more plant-based diet.

I reviewed the role endocrine-disrupting industrial pollutants in the food supply may play in a three-part video series: Fish and Diabetes, Diabetes and Dioxins, and Pollutants in Salmon and Our Own Fat. Clearly, the standard America diet and lifestyle contribute to the epidemic of diabetes and obesity, but the contribution of these industrial pollutants can no longer be ignored. We now have experimental evidence that exposure to industrial toxins alone induces weight gain and insulin resistance, and, therefore, may be an underappreciated cause of obesity and diabetes. Consider what's happening to our infants: Obesity in a six-month-old is obviously not related to diet or lack of exercise. They're now exposed to hundreds of chemicals from their moms, straight through the umbilical cord, some of which may be obesogenic (that is, obesity-generating).

The millions of pounds of chemicals and heavy metals released every year into our environment should make us all stop and think about how we live and the choices we make every day in the foods we eat. A 2014 review of the evidence on pollutants and diabetes noted that we can be exposed through toxic spills, but "most of the human exposure nowadays is from the ingestion of contaminated food as a result of bioaccumulation up the food chain. The main source (around 95%) of [persistent pollutant] intake is through dietary intake of animal fats."

For more on the information mentioned here, see the following videos that take a closer look at these major topics:

We've known that being overweight and obese are important risk factors for type 2 diabetes, but, until recently, not much attention has been paid to the role of specific foods. I discuss this issue in my video, Why Is Meat a Risk Factor for Diabetes?

A 2013 meta-analysis of all the cohorts looking at the connection between meat and diabetes found a significantly higher risk associated with total meat consumption--especially consumption of processed meat, particularly poultry. But why? There's a whole list of potential culprits in meat: saturated fat, animal fat, trans fats naturally found in meat, cholesterol, or animal protein. It could be the heme iron found in meat, which can lead to free radicals and iron-induced oxidative stress that may lead to chronic inflammation and type 2 diabetes, or advanced glycation end (AGE) products, which promote oxidative stress and inflammation. Food analyses show that the highest levels of these so-called glycotoxins are found in meat--particularly roasted, fried, or broiled meat, though any foods from animal sources (and even high fat and protein plant foods such as nuts) exposed to high dry temperatures can be potent sources of these pro-oxidant chemicals.

In another study, researchers fed diabetics glycotoxin-packed foods, like chicken, fish, and eggs, and their inflammatory markers--tumor necrosis factor, C-reactive protein, and vascular adhesion molecules--shot up. "Thus, in diabetes, environmental (dietary) AGEs promote inflammatory mediators, leading to tissue injury." The good news is that restriction of these kinds of foods may suppress these inflammatory effects. Appropriate measures to limit AGE intake, such as eliminating meat or using only steaming and boiling as methods for cooking it, "may greatly reduce the already heavy burden of these toxins in the diabetic patient." These glycotoxins may be the missing link between the increased consumption of animal fat and meats and the development of type 2 diabetes.

Since the 2013 meta-analysis was published, another study came out in which approximately 17,000 people were followed for about a dozen years. Researchers found an 8% increased risk for every 50 grams of daily meat consumption. Just one quarter of a chicken breast's worth of meat for the entire day may significantly increase the risk of diabetes. Yes, we know there are many possible culprits: the glycotoxins or trans fat in meat, saturated fat, or the heme iron (which could actually promote the formation of carcinogens called nitrosamines, though they could also just be produced in the cooking process itself). However, we did learn something new: There also appears to be a greater incidence of diabetes among those who handle meat for a living. Maybe there are some diabetes-causing zoonotic infectious agents--such as viruses--present in fresh cuts of meat, including poultry.

A "crucial factor underlying the diabetes epidemic" may be the overstimulation of the aging enzyme TOR pathway by excess food consumption--but not by the consumption of just any food: Animal proteins not only stimulate the cancer-promoting hormone insulin growth factor-1 but also provide high amounts of leucine, which stimulates TOR activation and appears to contribute to the burning out of the insulin-producing beta cells in the pancreas, contributing to type 2 diabetes. So, it's not just the high fat and added sugars that are implicated; critical attention must be paid to the daily intake of animal proteins as well.

According to a study, "[i]n general, lower leucine levels are only reached by restriction of animal proteins." To reach the leucine intake provided by dairy or meat, we'd have to eat 9 pounds of cabbage or 100 apples to take an extreme example. That just exemplifies the extreme differences in leucine amounts provided by a more standard diet in comparison with a more plant-based diet.

I reviewed the role endocrine-disrupting industrial pollutants in the food supply may play in a three-part video series: Fish and Diabetes, Diabetes and Dioxins, and Pollutants in Salmon and Our Own Fat. Clearly, the standard America diet and lifestyle contribute to the epidemic of diabetes and obesity, but the contribution of these industrial pollutants can no longer be ignored. We now have experimental evidence that exposure to industrial toxins alone induces weight gain and insulin resistance, and, therefore, may be an underappreciated cause of obesity and diabetes. Consider what's happening to our infants: Obesity in a six-month-old is obviously not related to diet or lack of exercise. They're now exposed to hundreds of chemicals from their moms, straight through the umbilical cord, some of which may be obesogenic (that is, obesity-generating).

The millions of pounds of chemicals and heavy metals released every year into our environment should make us all stop and think about how we live and the choices we make every day in the foods we eat. A 2014 review of the evidence on pollutants and diabetes noted that we can be exposed through toxic spills, but "most of the human exposure nowadays is from the ingestion of contaminated food as a result of bioaccumulation up the food chain. The main source (around 95%) of [persistent pollutant] intake is through dietary intake of animal fats."

For more on the information mentioned here, see the following videos that take a closer look at these major topics:

Do coffee drinkers live longer than non-coffee drinkers? Is it "wake up and smell the coffee" or don't wake up at all? I discuss these questions in my video, Coffee and Mortality.

The largest study ever conducted on diet and health put that question to the test, examining the association between coffee drinking and subsequent mortality among hundreds of thousands of older men and women in the United States. Coffee drinkers won, though the effect was modest, a 10-15% lower risk of death for those drinking six or more cups a day. This was due specifically to lower risk of dying from heart disease, respiratory disease, stroke, injuries and accidents, diabetes, and infections.

However, another study that amount of coffee was found to increase the death rate of younger people under age 55. It may be appropriate, then, to recommend that you avoid drinking more than four cups a day. But if you review all the studies, the bottom line is that coffee consumption is associated with no change or a small reduction in mortality starting around one or two cups a day, for both men and women. The risk of dying was 3% lower for each cup of coffee consumed daily, which provides reassurance for the concern that coffee drinking might adversely affect health, or at least longevity.

A recent population study found no link between coffee consumption and symptoms of GERD, reflux diseases such as heartburn and regurgitation. If you actually stick a tube down people's throats and measure pH, though, coffee induces significant acid reflux, whereas tea does not. Is this just because tea has less caffeine? No. If you reduce the caffeine content of the coffee down to that of tea, coffee still causes significantly more acid reflux. Decaf causes even less, so GERD patients might want to choose decaffeinated coffee or, even better, opt for tea.

Coffee intake is also associated with urinary incontinence, so a decrease in caffeine intake should be discussed with patients who have the condition. About two cups of coffee a day worth of caffeine may worsen urinary leakage.

A 2014 meta-analysis suggested that daily coffee consumption was associated with a slightly increased risk of bone fractures in women, but a decreased risk of fractures in men. However, no significant association was found between coffee consumption and the risk of hip fracture specifically. Tea consumption may actually protect against hip fracture, though it appears to have no apparent relationship with fracture risk in general.

Certain populations, in particular, may want to stay away from caffeine, including those with glaucoma or a family history of glaucoma, individuals with epilepsy, and, not surprisingly, people who have trouble sleeping. Even a single cup at night can cause a significant deterioration in sleep quality.

We used to think caffeine might increase the risk of an irregular heart rhythm called atrial fibrillation, but that was based on anecdotal case reports like one of a young woman who suffered atrial fibrillation after "chocolate intake abuse." These cases invariably involved the acute ingestion of very large quantities of caffeine. As a result, the notion that caffeine ingestion may trigger abnormal heart rhythms had become "common knowledge," and this assumption led to changes in medical practice.

We now have evidence that caffeine does not increase the risk of atrial fibrillation. Low-dose caffeine--defined as less than about five cups of coffee a day--may even have a protective effect. Tea consumption also appears to lower cardiovascular disease risk, especially when it comes to stroke. But given the proliferation of energy drinks that contain massive quantities of caffeine, one might temper any message that suggests that caffeine is beneficial. Indeed, 12 highly caffeinated energy drinks within a few hours could be lethal.

Do coffee drinkers live longer than non-coffee drinkers? Is it "wake up and smell the coffee" or don't wake up at all? I discuss these questions in my video, Coffee and Mortality.

The largest study ever conducted on diet and health put that question to the test, examining the association between coffee drinking and subsequent mortality among hundreds of thousands of older men and women in the United States. Coffee drinkers won, though the effect was modest, a 10-15% lower risk of death for those drinking six or more cups a day. This was due specifically to lower risk of dying from heart disease, respiratory disease, stroke, injuries and accidents, diabetes, and infections.

However, another study that amount of coffee was found to increase the death rate of younger people under age 55. It may be appropriate, then, to recommend that you avoid drinking more than four cups a day. But if you review all the studies, the bottom line is that coffee consumption is associated with no change or a small reduction in mortality starting around one or two cups a day, for both men and women. The risk of dying was 3% lower for each cup of coffee consumed daily, which provides reassurance for the concern that coffee drinking might adversely affect health, or at least longevity.

A recent population study found no link between coffee consumption and symptoms of GERD, reflux diseases such as heartburn and regurgitation. If you actually stick a tube down people's throats and measure pH, though, coffee induces significant acid reflux, whereas tea does not. Is this just because tea has less caffeine? No. If you reduce the caffeine content of the coffee down to that of tea, coffee still causes significantly more acid reflux. Decaf causes even less, so GERD patients might want to choose decaffeinated coffee or, even better, opt for tea.

Coffee intake is also associated with urinary incontinence, so a decrease in caffeine intake should be discussed with patients who have the condition. About two cups of coffee a day worth of caffeine may worsen urinary leakage.

A 2014 meta-analysis suggested that daily coffee consumption was associated with a slightly increased risk of bone fractures in women, but a decreased risk of fractures in men. However, no significant association was found between coffee consumption and the risk of hip fracture specifically. Tea consumption may actually protect against hip fracture, though it appears to have no apparent relationship with fracture risk in general.

Certain populations, in particular, may want to stay away from caffeine, including those with glaucoma or a family history of glaucoma, individuals with epilepsy, and, not surprisingly, people who have trouble sleeping. Even a single cup at night can cause a significant deterioration in sleep quality.

We used to think caffeine might increase the risk of an irregular heart rhythm called atrial fibrillation, but that was based on anecdotal case reports like one of a young woman who suffered atrial fibrillation after "chocolate intake abuse." These cases invariably involved the acute ingestion of very large quantities of caffeine. As a result, the notion that caffeine ingestion may trigger abnormal heart rhythms had become "common knowledge," and this assumption led to changes in medical practice.

We now have evidence that caffeine does not increase the risk of atrial fibrillation. Low-dose caffeine--defined as less than about five cups of coffee a day--may even have a protective effect. Tea consumption also appears to lower cardiovascular disease risk, especially when it comes to stroke. But given the proliferation of energy drinks that contain massive quantities of caffeine, one might temper any message that suggests that caffeine is beneficial. Indeed, 12 highly caffeinated energy drinks within a few hours could be lethal.

The phenomenon of postprandial angina was described more than 200 years ago: chest pain that occurs after a meal, even if you're just sitting down and resting. This could be intuitively attributed to redistribution of blood flow away from the heart to the gut during digestion. However, such a mechanism could not be demonstrated experimentally.

The problem appears to be within the coronary arteries themselves. The clue came in 1955 when researchers found they could induce angina in people with heart disease just by having them drink fat. My video Fatty Meals May Impair Artery Function includes a fascinating graph of so-called lactescence, or milkiness, over time. It shows how their blood became increasingly milky with fat over the next five hours, and each of the ten attacks of angina was found to occur about four-and-a-half to five hours after the fatty meal, right when blood milkiness was at or near its peak. After a nonfat meal with the same bulk and calories, but made out of starch, sugar, and protein, no anginal pain was elicited in any of the patients.

To understand how the mere presence of fat in the blood can affect blood flow to the heart, we need to understand the endothelium, the inner lining of all of our blood vessels. Our arteries are not just rigid pipes; they are living, breathing organs that actively dilate or constrict, thinning or thickening the blood and releasing hormones, depending on what's needed. This is all controlled by the single inner layer, the endothelium, which makes it the body's largest endocrine (hormone-secreting) organ. When it's all gathered up, the endothelium weighs a total of three pounds and has a combined surface area of 700 square yards.

We used to think the endothelium was just an inert layer lining our vascular tree, but now we know better:

Researchers found that low-fat meals tend to improve endothelial function, whereas high-fat meals tend to worsen it. This goes for animal fat, as well as isolated plant fats, such as sunflower oil. But, maybe it's just the digestion of fat rather than the fat itself? Our body can detect the presence of fat in the digestive tract and release a special group of hormones and enzymes. Researchers tried feeding people fake fat and found that the real fat deprived the heart of blood while the fake fat didn't. Is our body really smart enough to tell the difference?

A follow-up study settled the issue. Researchers tried infusing fat directly into people's bloodstream through an IV to sneak it past your mouth and brain. Within hours, their arteries stiffened, significantly crippling their ability to relax and dilate normally. So it was the fat after all! This decrease in the ability to vasodilate coronary arteries after a fatty meal, just when you need it, could explain the phenomenon of after-meal angina in patients with known coronary artery disease.

The phenomenon of postprandial angina was described more than 200 years ago: chest pain that occurs after a meal, even if you're just sitting down and resting. This could be intuitively attributed to redistribution of blood flow away from the heart to the gut during digestion. However, such a mechanism could not be demonstrated experimentally.

The problem appears to be within the coronary arteries themselves. The clue came in 1955 when researchers found they could induce angina in people with heart disease just by having them drink fat. My video Fatty Meals May Impair Artery Function includes a fascinating graph of so-called lactescence, or milkiness, over time. It shows how their blood became increasingly milky with fat over the next five hours, and each of the ten attacks of angina was found to occur about four-and-a-half to five hours after the fatty meal, right when blood milkiness was at or near its peak. After a nonfat meal with the same bulk and calories, but made out of starch, sugar, and protein, no anginal pain was elicited in any of the patients.

To understand how the mere presence of fat in the blood can affect blood flow to the heart, we need to understand the endothelium, the inner lining of all of our blood vessels. Our arteries are not just rigid pipes; they are living, breathing organs that actively dilate or constrict, thinning or thickening the blood and releasing hormones, depending on what's needed. This is all controlled by the single inner layer, the endothelium, which makes it the body's largest endocrine (hormone-secreting) organ. When it's all gathered up, the endothelium weighs a total of three pounds and has a combined surface area of 700 square yards.

We used to think the endothelium was just an inert layer lining our vascular tree, but now we know better:

Researchers found that low-fat meals tend to improve endothelial function, whereas high-fat meals tend to worsen it. This goes for animal fat, as well as isolated plant fats, such as sunflower oil. But, maybe it's just the digestion of fat rather than the fat itself? Our body can detect the presence of fat in the digestive tract and release a special group of hormones and enzymes. Researchers tried feeding people fake fat and found that the real fat deprived the heart of blood while the fake fat didn't. Is our body really smart enough to tell the difference?

A follow-up study settled the issue. Researchers tried infusing fat directly into people's bloodstream through an IV to sneak it past your mouth and brain. Within hours, their arteries stiffened, significantly crippling their ability to relax and dilate normally. So it was the fat after all! This decrease in the ability to vasodilate coronary arteries after a fatty meal, just when you need it, could explain the phenomenon of after-meal angina in patients with known coronary artery disease.

The recent film What the Health raised the question as to whether sugar or other carbohydrates cause diabetes. Because blood sugar levels are high in diabetes, a common notion has held that eating sugar somehow triggers the disease process. The... Read more